Researchers from Karolinska Institutet have discovered a new molecular mechanism by which cancer cells safeguard themselves from oncogene-induced replication stress and propose a strategy to deactivate this protective mechanism. The study is published in the journal Molecular Cell.
Researchers from Karolinska Institutet have discovered a new molecular mechanism by which cancer cells safeguard themselves from oncogene-induced replication stress and propose a strategy to deactivate this protective mechanism. The study is published in the journalThe study has revealed an unanticipated mechanism responsible for the removal of a pivotal DNA repair protein, FANCD2, at stopped replication forks.
"Our cells face continuous DNA damage, especially during DNA synthesis governed by cyclin-dependent kinases . Elevated CYCLIN E levels are associated with aggressive cancer types and unfavorable patient prognoses, posing inherent treatment challenges. From a clinical standpoint, CYCLIN E is not perceived as a feasible drug target.
"We initiated the study by carrying out a screen for genes regulating recovery of replication in cancer cells that overexpress CYCLIN E and identified FBXL12 as a prominent candidate. Employing high-resolution microscopy of individual DNA molecules and replication tracks, we next investigated how FBXL12 influences replication fork dynamics," Olle Sangfelt, the study's senior author says.
"Based on our findings, we propose that the disruption of FBXL12-FANCD2 signaling renders cells overexpressing CYCLIN E nonviable and hypothesize that targeting this pathway, alongside other cancer drugs inducing replication stress, may offer a feasible treatment avenue also for cancer types devoid of elevated replication stress levels.
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